Stroke represents a leading cause of non-traumatic prolonged disorders of consciousness (pDoC). Given the prefrontal cortex's critical role in consciousness, this study aimed to explore the abnormalities in the prefrontal network in post-stroke pDoC patients. Using resting-state functional near-infrared spectroscopy (fNIRS), we acquired data from 21 post-stroke pDoC patients and 19 age- and gender-matched healthy controls (HC). Based on the Coma Recovery Scale-Revised, patients were classified into 12 with minimally conscious state (MCS) and 9 with unresponsive wakefulness syndrome (UWS). We analyzed and compared functional connectivity and topological properties of the prefrontal network across groups. Compared to HCs, the pDoC group exhibited extensively weakened functional connectivity and disrupted network topology, as evidenced by a lower clustering coefficient (Cp), reduced local efficiency (Eloc), global efficiency (Eg) and a longer characteristic path length (Lp). Reductions in key nodal metrics which including nodal clustering coefficient (NCp), nodal efficiency (Ne), and degree centrality (DC) were also observed across several prefrontal regions. In the direct comparison between patient subgroups, the MCS group demonstrated significantly stronger functional connectivity within the right premotor and supplementary motor cortex (PreM & SMA_R) than the UWS group, but conversely, showed weaker connectivity within the left frontopolar area (FPA_L). Consequently, assessing prefrontal network integrity with portable fNIRS holds promise for identifying potential biomarkers to diagnose and monitor post-stroke prolonged disorders of consciousness.

Neuroplasticity plays a pivotal role in post-stroke recovery, and Angelica sinensis polysaccharide has demonstrated neuroprotective properties. This study investigated the neuroprotective effects of low-molecular-weight Angelica sinensis polysaccharide (LMW-ASP) in a rat middle cerebral artery occlusion/reperfusion (MCAO/R) model. Structural characterization revealed that LMW-ASP (3.9 kDa), containing a pyranose ring and uronic acid, was a heteropolysaccharide that comprised fucose, galactosamine hydrochloride, rhamnose, arabinose, glucosamine hydrochloride, galactose, glucose, xylose, mannose, galacturonic acid, and glucuronic acid (0.007:0.003:0.057:0.209:0.009:0.284:0.303:0.006:0.032:0.083:0.007). Post-stroke administration of LMW-ASP (50 mg/kg) significantly improved body weight and neurological functions after MCAO/R. Moreover, microtubule-associated protein-2 expression was notably higher in the LMW-ASP group than in the model group (p < 0.01). Furthermore, Golgi-Cox staining confirmed that LMW-ASP increased the number of dendritic intersections (p < 0.05 for 90-120, 180, and 200 μm; p < 0.001 for 70 and 80 μm), the number of terminal branches (p < 0.01), the number of branch points (p < 0.01), and the density of basal dendritic spines (p < 0.05). Finally, transmission electron microscopy revealed an increase in the number of synapses (p < 0.001) and presynaptic vesicles (p < 0.001) in the LMW-ASP group. These results suggest that LMW-ASP is a potential pharmaceutical therapeutic approach for stroke recovery that enhances neuroplasticity.

Tetramethylpyrazine (TMP) is an active component of the Chuanxiong, effectively crosses blood-brain barrier (BBB). It exhibits neuroprotective potential in cerebral ischemia-reperfusion injury (CIRI). This study performed middle cerebral artery occlusion/reperfusion (MCAO/R) surgery in rats to evaluate TMP’s efficacy and mechanisms in mitigating CIRI. Rats received intraperitoneal TMP (40 mg/kg) for 3 days prior to MCAO/R and continued for 14 days post-surgery. Behavioral tests were conducted using mNSS and Morris water maze tests. Histopathological analyses, including HE, Nissl, and TUNEL staining. mRNA sequencing revealed that RhoA and ROCK2 were upregulated in the CIRI model and downregulated by TMP treatment. GO enrichment and KEGG enrichment showed RhoA and ROCK were related to neuroplasticity. Western blot and immunofluorescence staining confirmed that TMP inhibited RhoA, ROCK2, phosphorylated LIMK, and phosphorylated cofilin expression. Additionally, TMP increased the levels of neuroplasticity-related proteins PSD95 and MAP2, promoting synaptic and dendritic regeneration. Administration of lysophosphatidic acid (LPA), a RhoA/ROCK pathway agonist, attenuated TMP’s neuroprotective effects, validating the pathway’s role in TMP-mediated protection. These findings indicate that TMP confers neuroprotection in CIRI by inhibiting the RhoA/ROCK pathway and enhancing neuroplasticity, underscoring its therapeutic potential in CIRI.

Introduction Poststroke cognitive impairment is a common complication in stroke survivors, seriously affecting their quality of life. Therefore, it is crucial to improve cognitive function of patients who had a stroke. Transcranial direct current stimulation (tDCS) and transcutaneous auricular vagus nerve stimulation (taVNS) are non-invasive, safe treatments with great potential to improve cognitive function in poststroke patients. However, further improvements are needed in the effectiveness of a single non-invasive brain stimulation technique for cognitive rehabilitation. This study protocol aims to investigate the effect and neural mechanism of the combination of tDCS and taVNS on cognitive function in patients who had a stroke.Methods and analysis In this single-centre, prospective, parallel, randomised controlled trial, a total of 66 patients with poststroke cognitive impairment will be recruited and randomly assigned (1:1:1) to the tDCS group, the taVNS group and the combination of tDCS and taVNS group. Each group will receive 30 min of treatment daily, five times weekly for 3 weeks. Primary clinical outcome is the Montreal Cognitive Assessment. Secondary clinical outcomes include the Mini-Mental State Examination, Stroop Colour Word Test, Trail Marking Test, Symbol Digit Modalities Test and Modified Barthel Index. All clinical outcomes, functional MRI and diffusion tensor imaging will be measured at preintervention and postintervention.Ethics and dissemination The trial has been approved by the Ethics Committee of the First Affiliated Hospital of Yangtze University (approval no: KY202390). The results will be submitted for publication in peer-reviewed journals or at scientific conferences.Trial registration number ChiCTR2300076632.

Chronic cerebral hypoperfusion (CCH) is a primary contributor to cognitive decline in the elderly. Enriched environment (EE) is proved to improve cognitive function. However, mechanisms involved remain unclear. The purpose of the study was exploring the mechanisms of EE in alleviating cognitive deficit in rats with CCH. To create a rat model of CCH, 2-vessel occlusion (2-VO) surgery was performed. All rats lived in standard or enriched environments for 4 weeks. Cognitive function was assessed using the novel object recognition test and Morris water maze test. The protein levels of glutamatergic synapses, neurotoxic reactive astrocytes, reactive microglia, and JAK2-STAT3 signaling pathway were measured using Western blot. The mRNA levels of synaptic regulatory factors, C1q, TNF-α, and IL-1α were identified using quantitative PCR. Immunofluorescence was used to detect glutamatergic synapses, neurotoxic reactive astrocytes, and reactive microglia, as well as the expression of p-STAT3 in astrocytes in the hippocampus. The results demonstrated that the EE mitigated cognitive impairment in rats with CCH and enhanced glutamatergic synaptogenesis. EE also inhibited the activation of neurotoxic reactive astrocytes. Moreover, EE downregulated microglial activation, levels of C1q, TNF-α and IL-1α and phosphorylation of JAK2 and STAT3. Our results suggest that inhibition of neurotoxic reactive astrocytes may be one of the mechanisms by which EE promotes glutamatergic synaptogenesis and improves cognitive function in rats with CCH. The downregulation of reactive microglia and JAK2-STAT3 signaling pathway may be involved in this process.

A typical enriched environment (EE), which combines physical activity and social interaction, has been proven to mitigate cognitive impairment caused by chronic cerebral hypoperfusion (CCH). However, it remains unclear how the different components of EE promote cognitive recovery after CCH. This study stripped out the different components of EE into physical environmental enrichment (PE) and social environmental enrichment (SE), and compared the neuroprotective effects of PE, SE and typical EE (PSE) in CCH. The results of novel object recognition and Morris water maze tests showed that PE, SE, and PSE improved cognitive function in CCH rats. Additionally, Nissl and TUNEL staining revealed that three EEs reduced neuronal loss in the hippocampus. PSE exhibited superior neuroprotective and functional improvement effects compared to PE and SE, while there was no significant difference between PE and SE. Furthermore, three EEs reduced lipid peroxidation in the hippocampus with decreasing the levels of MDA and increasing the activities of SOD and GSH. The expression of SLC7A11 and GPX4 was increased, while the level of p53 was reduced in three EEs. This suggested that three EEs inhibited ferroptosis by maintaining the redox homeostasis in the hippocampus. Three EEs reduced the levels of IL-β, TNF-α, and IL-6, thereby inhibiting neuroinflammation. Additionally, Western blotting and immunofluorescence results indicated that three EEs also inhibited the TLR4/MyD88/p38MAPK signaling pathway. These findings collectively demonstrated that the three EEs alleviated hippocampal ferroptosis and neuroinflammation in CCH rats, thereby reducing neuronal loss, which might be associated with the inhibition of the TLR4/MyD88/p38MAPK signaling pathway. Moreover, the study results supported that it is only through the combination of physical exercise and social interaction that the optimal neuroprotective effects can be achieved. These findings provided valuable insights for the prevention and treatment of vascular cognitive impairment.

Preventing neuronal death after ischemic stroke (IS) is crucial for neuroprotective treatment, yet current management options are limited. Enriched environment (EE) is an effective intervention strategy that promotes the recovery of neurological function after cerebral ischemia/reperfusion (I/R) injury. Ferroptosis has been identified as one of the mechanisms of neuronal death during IS, and inhibiting ferroptosis can reduce cerebral I/R injury. Our previous research has demonstrated that EE reduced ferroptosis by inhibiting lipid peroxidation, but the underlying mechanism still needs to be investigated. This study aims to explore the potential molecular mechanisms by which EE modulates iron metabolism to reduce ferroptosis. The experimental animals were randomly divided into four groups based on the housing environment and the procedure the animals received: the sham-operated + standard environment (SSE) group, the sham-operated + enriched environment (SEE) group, the ischemia/reperfusion + standard environment (ISE) group, and the ischemia/reperfusion + enriched environment (IEE) group. The results showed that EE reduced IL-6 expression during cerebral I/R injury, hence reducing JAK2-STAT3 pathway activation and hepcidin expression. Reduced hepcidin expression led to decreased DMT1 expression and increased FPN1 expression in neurons, resulting in lower neuronal iron levels and alleviated ferroptosis. In addition, EE also reduced the expression of TfR1 in neurons. Our research suggested that EE played a neuroprotective role by modulating iron metabolism and reducing neuronal ferroptosis after cerebral I/R injury, which might be achieved by inhibiting inflammatory response and down-regulating hepcidin expression.

Enriched environment (EE) has been proven to be an effective intervention strategy which can improve neurofunctional recovery following cerebral ischemia/reperfusion (I/R) injury. However, it still needs further investigation for the underlying mechanisms. Recently, it has been shown that ferroptosis played an essential role in the pathophysiological development of ischemic stroke (IS). This study is aimed at investigating whether EE plays a neuroprotective role by attenuating ferroptosis after cerebral I/R injury. We used middle cerebral artery occlusion/reperfusion (MCAO/R) to build a model of cerebral I/R injury. To evaluate the effect of EE on neurological recovery, we used the modified neurological severity score (mNSS) and the Morris water maze (MWM). We used the western blot to detect the protein levels of glutathione peroxidase 4 (GPX4), hypoxia-inducible factor-1α (HIF-1α), and acyl-CoA synthetase long-chain family member 4 (ACSL4). We used the quantitative real-time PCR (qRT-PCR) to measure the mRNA levels of ACSL4 and inflammatory cytokines including tumor necrosis factor alpha (TNFα), interleukin-6 (IL-6), and interleukin 1 beta (IL-1β). The occurrence of ferroptosis was detected by TdT-mediated dUTP nick-end labeling (TUNEL) assay, diaminobenzidine- (DAB-) enhanced Perls’ staining, iron level assays, and malondialdehyde (MDA) level assays. The results verified that EE enhanced functional recovery and attenuated ferroptosis and neuroinflammation after cerebral I/R injury. EE increased the expression of HIF-1α while inhibited the expression of ACSL4. Our research indicated that EE improved functional recovery after cerebral I/R injury through attenuating ferroptosis, and this might be related to its regulation of the neuroinflammation and HIF-1α-ACSL4 pathway.

Background: The clinical applications of stromal vascular fraction (SVF) therapy for osteoarthritis (OA) have attracted academic and clinical attention. However, data of the effects of stromal vascular fraction therapy on regeneration of degenerated cartilage are limited in the literature. Meanwhile, there is a great need for a simple and non-invasive evaluation method to analyze the changes of joint cartilage qualitatively and quantitatively in clinical trials. This study entitled “stromal vascular fraction Therapy for Human Knee Osteoarthritis” was registered in ClinicalTrial.gov # NCT05019378.Materials and Methods: We designed and conducted a single center, open labeled clinical phase I/II study, and 6 osteoarthritis patients with both knee cartilage defect I-II were enrolled in this study. The two knees of each patient were randomly assigned to autologous stromal vascular fraction treatment group or non-treatment control group to evaluate the safety and therapeutic effect of stromal vascular fraction therapy for human knee osteoarthritis. We have also established a novel protocol to provide 3D MRI imaging for human knee cartilage enabling us to qualitatively and quantitatively evaluate cartilage degeneration and regeneration in this study.Results: The qualitative and quantitative evaluation of 3D Magnetic Resonance Imaging (MRI) imaging of knee cartilage demonstrated that the stromal vascular fraction therapy reduced the cartilage defects; and significant increase of cartilage value both in defect cartilage area and whole cartilage area of treated group and significant increase of thickness and area of both femoral and tibia cartilage in vertical sections of the stromal vascular fraction treated Group at 12 and 24 W post treatment in cartilage defect I-II osteoarthritis patients.Conclusion: This clinical phase I/II study indicated that stromal vascular fraction therapy is a safe clinical procedure and provided evidence that the stromal vascular fraction therapy significantly facilitated cartilage regeneration, opening the opportunity to a phase III trial investigating authentic efficacy of the procedure. This study is the first qualitative and quantitative evaluation of the efficacy of autologous stromal vascular fraction cellular therapy on cartilage regeneration. Through early and definite diagnosis of knee osteoarthritis patients, and providing safe and efficient therapy to facilitate cartilage regeneration, we will be able to control or reverse cartilage degeneration and completely change the epidemiology of osteoarthritis worldwide.

Background Patients in minimally conscious state (MCS) exist measurable evidence of consciousness. The frontal lobe is a crucial part of the brain that encodes abstract information and is closely related to the conscious state. We hypothesized that the disturbance of the frontal functional network exists in MCS patients. Methods We collected the resting-state functional near-infrared spectroscopy (fNIRS) data of fifteen MCS patients and sixteen age- and gender-matched healthy controls (HC). The Coma Recovery Scale-Revised (CRS-R) scale of MCS patients was also composed. The topology of the frontal functional network was analyzed in two groups. Results Compared with HC, the MCS patients showed widely disrupted functional connectivity in the frontal lobe, especially in the frontopolar area and right dorsolateral prefrontal cortex. Moreover, the MCS patients displayed lower clustering coefficient, global efficiency, local efficiency, and higher characteristic path length. In addition, the nodal clustering coefficient and nodal local efficiency in the left frontopolar area and right dorsolateral prefrontal cortex were significantly reduced in MCS patients. Furthermore, the nodal clustering coefficient and nodal local efficiency in the right dorsolateral prefrontal cortex were positively correlated to auditory subscale scores. Conclusion This study reveals that MCS patients’ frontal functional network is synergistically dysfunctional. And the balance between information separation and integration in the frontal lobe is broken, especially the local information transmission in the prefrontal cortex. These findings help us to understand the pathological mechanism of MCS patients better.

Objective:To explore the characteristics of functional connectivity (FC) and regional spontaneous brain activity in patients in a minimally-conscious state (MCS).Methods:Resting-state functional near-infrared spectroscopy (rs-fNIRS) was used. Ten minimally-conscious patients were studied along with 12 healthy counterparts as healthy controls (HC). Five minutes of rs-fNIRS data were recorded from each subject and FC and the fractional amplitude of low-frequency fluctuations (fALFFs) of 53 channels were computed using the NIRS-KIT toolbox. The results were compared between the two groups.Results:Compared with the HC group, a significant decrease was observed in the average FC strength of seventeen channel pairs after false discovery rate (FDR) correction. Most were in the right and left frontal pole, as well as the dorsolateral prefrontal lobe. Compared with the HC group, the average fALFF values of Broca′s area (channel 2), the premotor cortex and the supplementary motor cortex (channels 4, 10, and 40), the dorsolateral prefrontal lobe (channels 6, 11, 25, 39), the eye motor area of the frontal lobe (channel 12) and the frontal pole (channels 23, 27, 36) were significantly greater in the MCS group. The fluctuations of the frontal pole (channel 19) were significantly less (after FDR correction).Conclusion:In an MCS spontaneous neural activity is over-active in the prefrontal lobe and some speech- and motor-related brain regions, and coordination of the internal prefrontal functional network is disordered.

脑血管疾病在我国的发病率逐年提升,其高发病率、病死率及致残率给社会及家庭带来了巨大的经济压力与负担[1],其中重症脑血管疾病因病变面积较大,涉及多脑叶或重要区域,常伴有呼吸困难、吞咽障碍、肺部感染等严重并发症,而早期气管切开是重要的生命支持措施之一[2],但由于气管切开后气道阻力下降,吞咽时无法形成声门下气压,部分患者合并吞咽障碍并带有鼻饲管,常常难以拔管甚至需终身带管生活[3].

目的:研究间歇性θ短阵快速脉冲刺激(iTBS)对氧糖剥夺/再灌注(OGD/R)引起的小胶质细胞极化和炎症反应的影响及潜在分子机制.方法:将iTBS作用于BV2小胶质细胞OGD/R体外模型,1次/d,连续干预3d,在第4天收集所有样本进行检测.采用光学显微镜观察形态学的变化,实时荧光定量PCR检测炎症因子mRNA表达水平,流式细胞术和免疫荧光检测小胶质细胞M1/M2标记物的表达,蛋白免疫印迹法检测总NF-κB p65和磷酸化NF-κB p65(p-p65)、总STAT3和磷酸化STAT3(p-STAT3)蛋白表达水平.结果:OGD/R损伤后,BV2细胞由梭形向阿米巴样转变,但经iTBS 干预后,细胞形态无明显变化.与假刺激组相比,iTBS 明显降低了促炎因子TNF-α、IL-1β、IL-6、iNOS 和Mcp-1 的mRNA表达水平(P＜0.05),升高了抗炎因子TGF-β1、IL-10和Arg-1 的mRNA表达水平(P＜0.05).此外,iTBS显著降低了M1标记物CD16/32、CD86的表达(P＜0.05)和增加了M2标记物CD206、CD163的表达(P＜0.05).同时,经iTBS干预后,BV2小胶质细胞p-p65的蛋白表达水平显著下调(P＜0.05),p-STAT3的蛋白表达水平显著上调(P＜0.05).结论:iTBS可减轻OGD/R诱导的小胶质细胞相关神经炎症,其中的机制可能是iTBS通过抑制p-p65和上调p-STAT3的表达参与调控NF-κB和STAT3通路,进而调节小胶质细胞极化,诱导其由促炎型M1 向抗炎型M2转化.

The purpose of this study was to investigate the efficacy of Kinesio taping (KT) combined with multi-angle isometric resistance training for cervical spondylosis. Sixty-one patients were divided into two groups by random number table method. Both groups were given multi-angle isometric training, the patients in the observation group were supplemented with Kinesio taping. Before and after treatment, the symptoms of cervical spine function were evaluated in two groups by visual analogue scale (VAS), cervical dysfunction index (NDI), cervical range of motion and muscle stiffness. After 3 weeks of treatment, VAS, NDI scores and the cervical range of motion were significantly better than before (P < 0.05). The range of anterior flexion and extension was significantly larger than the control group (P < 0.05), but the range of other motions were not certain. The muscle stiffness in KT group were significantly lower than the control group. Kinesio taping combined with multi-angle isometric resistance training can further alleviate the clinical symptoms and correct the neck abnormal posture. But its effects on the range of cervical motion remain uncertain.

Objective:To explore any changes in the topology of the brain′s resting-state functional networks after an ischemic stroke causing cognitive impairment (iPSCI) and their relationship with the impairment.Methods:Twenty-one patients with impaired cognition after a stroke were recruited into an iPSCI group, and 21 healthy counterparts matched in gender, age and the education level formed the control (HC) group. Three-dimensional T1-weighted anatomical images and resting state functional magnetic resonance images of all of the subjects were collected and any differences in brain network topology were analyzed using graph theory. The degree of centrality (DC), between centrality (BC) and the global topological properties of each brain region were compared using independent-sample t-tests. Spearman correlation coefficients were computed to analyze the significance of any correlation between topology differences and Montreal Cognitive Assessment Scale (MoCA) or Mini-Mental Status Examination (MMSE) scores.Results:Compared with the HC group, a significant DC increase was observed in the orbital part of the right of middle frontal gyrus (ORBmid.R), the right hippocampus (HIP.R), and the right thalamus (THA.R). There was a significant decrease in the left Rolandic operculum (ROL.L), the left postcentral gyrus (PoCG.L), the left supramarginal gyrus (SMG.L), the left angular gyrus (ANG.L), the left and right caudate nucleus (CAU.L and CAU.R), the putamen of the left lenticular nucleus (PUT.L), the left Heschl gyrus (HES.L), the left superior temporal gyrus (STG.L), and the temporal pole of the left superior temporal gyrus (TPOsup.L). Compared with the HC group, the brain regions of the iPSCI group in which the BC had increased significantly were the orbital part of the left middle frontal gyrus (ORBmid.L), the left cuneus (CUN.L), and the right precuneus (PCUN.R). DC was significantly decreased in the left caudate nucleus (CAU.L), the left temporal pole of the superior temporal gyrus (TPOsup.L), and the left of inferior temporal gyrus (ITG.L). Compared with the HC group, the area under the receiver operating curve (AUC) of the shortest path length (Lp) and the normalized Lp (λ) of the iPSCI group increased significantly, and the AUC of the normalized clustering coefficient (γ) and small-worldness (σ) decreased significantly. The DCs of the ROL.L, PoCG.L, CAU.L, HES.L, STG.L and TPOsup.L regions showed moderate positive correlation with the MoCA and MMSE scores ( r>0.4), as did the BC of the CAU.L and TPOsup.L regions ( r>0.4). Conclusions:Cognitive impairment is mainly associated with decreased nodal properties in the brain regions related to language and in the caudate nucleus. The topology of the frontal lobe, hippocampus, thalamus, striatum and default networks may self-repair after an iPSCI. The brain′s functional network after an iPSCI still has small-world properties, but with low efficiency and high cost.

Chronic cerebral hypoperfusion (CCH) is closely related to vascular cognitive impairment and dementia (VCID) and Alzheimer's disease (AD). The neuroinflammation involving astrocytes is an important pathogenic mechanism. Along with the advancement of the concept and technology of astrocytic biology, the astrocytes have been increasingly regarded as the key contributors to neurological diseases. It is well known that physical exercise can improve cognitive function. As a safe and effective non-drug treatment, physical exercise has attracted continuous interests in neurological research. In this study, we explored the effects of physical exercise on the response of reactive astrocytes, and its role and mechanism in CCH-induced cognitive impairment. A rat CCH model was established by 2 vessel occlusion (2VO) and the wheel running exercise was used as the intervention. The cognitive function of rats was evaluated by morris water maze and novel object recognition test. The phenotypic polarization and the primary cilia expression of astrocytes were detected by immunofluorescence staining. The activation of MAPKs cascades, including ERK, JNK, and P38 signaling pathways, were detected by western blot. The results showed that physical exercise improved cognitive function of rats 2 months after 2VO, reduced the number of C3/GFAP-positive neurotoxic astrocytes, promoted the expression of S100A10/GFAP-positive neuroprotective astrocytes, and enhanced primary ciliogenesis. Additionally, physical exercise also alleviated the phosphorylation of ERK and JNK proteins induced by CCH. These results indicate that physical exercise can improve the cognitive function of rats with CCH possible by promoting primary ciliogenesis and neuroprotective function of astrocytes. The MAPKs signaling cascade, especially ERK and JNK signaling pathways may be involved in this process.

The topology of brain networks is the foundation of cognition. We hypothesized that stroke damaged topological organization resulting in cognitive impairment. The aim was to explore the damage pattern of the resting-state topology in post-stroke cognitive impairment (PSCI) patients. Thirty-seven patients with PSCI and thirty-seven gender- and age-matched healthy controls (HC) were recruited. The structural and functional data were collected from all subjects. The degree centrality (DC), betweenness centrality (BC), and global properties of brain networks were analyzed between groups. Spearman correlation analysis was performed between topological properties that changed significantly and clinical cognitive function scale scores. Compared with HC, the PSCI patients had significantly reduced DC in language-related brain regions and significantly higher DC in the right frontal lobe, hippocampus, and paracentral lobule. The decreased BC was located in the left caudate, thalamus, temporal, and frontal lobes. The increased BC was detected in the left cuneus and right precuneus. In addition, PSCI exhibited increased characteristic path length and decreased small-worldness. PSCI patients had impaired functional topology of the language-related brain regions, mainly in the left hemisphere. The enhanced processing and relaying information of some right high-order cognitive brain regions may be a compensatory mechanism. However, the whole brain's function integration was reduced, and there was an imbalance between efficiency and consumption.

Objective:To understand the interest in and influencing factors of cognitive rehabilitation for interns from rehabilitation therapeutics interns.Methods:A total of 169 interns from rehabilitation therapeutics major who practiced in the department of neurorehabilitation, Zhongnan Hospital of Wuhan University from 2020 to 2022 were selected as study subjects. A questionnaire was used to investigate their interest, cognitive status and influencing factors in cognitive rehabilitation. Chi-square test and logistic regression analysis were used for statistical analysis.Results:A total of 57.4% (97/169) of the interns were interested in cognitive impairment rehabilitation. The top three cognitive domains they were interested in were memory [65.0%(63/97)], attention [60.8%(59/97)] and executive dysfunction [48.5%(47/97)]. Compared with the dispensing student, the students who volunteered to fill in the rehabilitation major were more interested in cognitive rehabilitation ( OR=3.41, 95% CI: 1.46~7.99); Students who rotated in the cognitive therapy room were also more interested in cognitive rehabilitation than students who did not rotate ( OR=2.28, 95% CI: 1.12~4.63), the differences were statistically significant (all P<0.05). Conclusions:Rehabilitation therapeutics interns are generally interested in cognitive rehabilitation. It is necessary to further strengthen faculty development of teachers in cognitive rehabilitation, improve their clinical professional ability and teaching level, expand students′ knowledge acquisition pathways and clinical practice opportunities and actively explore diversified teaching modes, so as to increase students′ interest and learning intentions in cognitive rehabilitation.

BackgroundStroke is an important cause of cognitive impairment. Rich club organization, a highly interconnected network brain core region, is closely related to cognition. We hypothesized that the disturbance of rich club organization exists in patients with post-stroke cognitive impairment (PSCI).MethodsWe collected data on resting-state functional magnetic resonance imaging (rs-fMRI) with 21 healthy controls (HC), 16 hemorrhagic stroke (hPSCI), and 21 infarct stroke (iPSCI). 3D shape features and first-order statistics of stroke lesions were extracted using 3D slicer software. Additionally, we assessed cognitive function using the Montreal Cognitive Assessment (MoCA) and Mini-Mental State Examination (MMSE).ResultsNormalized rich club coefficients were higher in hPSCI and iPSCI than HC at low-degree k-levels (k = 1–8 in iPSCI, k = 2–8 in hPSCI). Feeder and local connections were significantly decreased in PSCI patients versus HC, mainly distributed in salience network (SN), default-mode network (DMN), cerebellum network (CN), and orbitofrontal cortex (ORB), especially involving the right and left caudate with changed nodal efficiency. The feeder and local connections of significantly between-group difference were positively related to MMSE and MoCA scores, primarily distributed in the sensorimotor network (SMN) and visual network (VN) in hPSCI, SN, and DMN in iPSCI. Additionally, decreased local connections and low-degree ϕnorm(k) were correlated to 3D shape features and first-order statistics of stroke lesions.ConclusionThis study reveals the disrupted low-degree level rich club organization and relatively preserved functional core network in PSCI patients. Decreased feeder and local connections in cognition-related networks (DMN, SN, CN, and ORB), particularly involving the caudate nucleus, may offer insight into pathological mechanism of PSCI patients. The shape and signal features of stroke lesions may provide an essential clue for the damage of functional connectivity and the whole brain networks.

功能性近红外光谱成像技术(fNIRS)可作为脑卒中患者治疗过程中的神经反馈工具、辅助诊断和疗效评估工具，本文旨在通过总结fNIRS在脑卒中后伴有抑郁、认知障碍、吞咽障碍和失语症的相关研究，以期为脑卒中后非运动障碍的康复提供借鉴和参考。